Kojima I, Shibata H, Ogata E
J Biol Chem. 1987 Apr 5;262(10):4557-63.
In adrenal glomerulosa cells, angiotensin II causes an immediate release of calcium from an intracellular trigger pool (Kojima, I., Kojima, K., and Rasmussen, H. (1985) Am. J. Physiol. 247, E36-E43). The present study was conducted to determine how the trigger pool of calcium is restored after cessation of the agonist action. Upon termination of angiotensin II action, calcium influx rate decreased immediately while total cell calcium increased rapidly. The increase in total cell calcium is not affected by 1 microM nitrendipine, which blocks angiotensin II-stimulated calcium influx without inhibiting basal influx of calcium. In contrast, total cell calcium did not increase in medium containing 1 microM calcium, in which basal calcium influx is negligible. A rapid increase in total cell calcium after an addition of the antagonist was not accompanied by changes in cytoplasmic free calcium concentration. A second stimulation of cells with either angiotensin II or carbachol did not cause calcium release when the interval of two stimulations was shorter than 20 min. The longer the interval, the greater the magnitude of calcium release in response to the second stimulator. The maximum response was obtained when the interval was 40 min or more. When exogenous arachidonic acid, which mobilized calcium by acting directly on the inositol trisphosphate-sensitive pool, was employed as a second stimulator, the magnitude of the decrease in total cell calcium was also dependent on the interval. These results suggest that, upon termination of angiotensin II action, calcium is rapidly accumulated first in an intracellular pool which is insensitive to either inositol 1,4,5-trisphosphate or arachidonic acid and that the trigger pool is restored gradually thereafter.
在肾上腺球状带细胞中,血管紧张素II可使细胞内触发池立即释放钙(小岛一、小岛克和拉斯穆森,H.(1985年)《美国生理学杂志》247卷,E36 - E43页)。本研究旨在确定激动剂作用停止后钙触发池是如何恢复的。血管紧张素II作用终止后,钙内流速率立即下降,而细胞总钙含量迅速增加。细胞总钙含量的增加不受1微摩尔尼群地平的影响,尼群地平可阻断血管紧张素II刺激的钙内流而不抑制基础钙内流。相反,在含有1微摩尔钙的培养基中,细胞总钙含量并未增加,在该培养基中基础钙内流可忽略不计。加入拮抗剂后细胞总钙含量迅速增加,同时细胞质游离钙浓度并未改变。当两次刺激的间隔短于20分钟时,用血管紧张素II或卡巴胆碱对细胞进行第二次刺激不会引起钙释放。间隔时间越长,对第二次刺激物的钙释放量越大。当间隔为40分钟或更长时间时可获得最大反应。当使用外源性花生四烯酸作为第二次刺激物时,花生四烯酸通过直接作用于肌醇三磷酸敏感池来动员钙,细胞总钙含量的下降幅度也取决于间隔时间。这些结果表明,血管紧张素II作用终止后,钙首先迅速积累在一个对肌醇1,4,5 - 三磷酸或花生四烯酸均不敏感的细胞内池中,随后触发池逐渐恢复。